Alterations in body fluid metabolism that result in relative deficiencies of water or sodium produce compensatory increases in thirst and sodium appetite, respectively. The general aim of my research is to understand the physiological bases for these drives, and their integration with complementary physiological contributions to homeostasis. In the past year I have abandoned the traditional view of thirst and sodium appetite as being stimulated by alterations in specific body fluid compartments, and now view the stimuli for these drives from the perspective of the changes they cause in the activity of neuronal systems mediating cerebral arousal. Central catecholamine-containing neurons have been demonstrated to be of critical importance to behavioral activation, and it is stimulation of these neurons during thirst that provides the present model for motivation. The specific aims of the proposed research are to evaluate this model by determining (i) the effect of thirst stimuli on activity in central catecholaminergic neurons, (ii) whether administration of caffeine would reverse the deficits in thirst that are caused by destruction of central catecholaminergic neurons, (iii) the effect of changes in plasma sodium or angiotensin levels on sodium appetite in rats, (iv) the effect of destroying central serotonergic neurons on thirst, and (v) the effects of hypovolemia on thirst and sodium appetite in sheep.